Preparation from the gum resin of Boswellia serrata have been used as a traditional remedy in Indian medicine in India for the treatment of inflammatory diseases. Compounds from the gum with genuine anti-inflammatory effects are pentacyclic triterpenes of the boswellic acid type. Boswellic acids inhibit the leukotriene biosynthesis in neutrophilic granulocytes by a non-redox, noncompetitive inibition of 5-lipoxy genase. The effect is triggered by boswellic acids binding to the enzyme. Moreover certain boswellic acids have been described to inhibit elastase in leukoeytes, to inhibit proliferation, induce apoptosis and to inhibit topoisomerases of leukoma and glioma cell lines. A series of chronic inflammatory diseases are thought to be perpetuated by leukotrienes. In clinical trials promissing results were observed in patients with rheumatoid arthritis, chronic colitis, ulcerative colitis, Crohn’s disease, bronchial asthma and peritumoral brains edemas.

Human Genome Screen to Identify the Genetic Basis of the Anti-inflammatory Effects of Boswellia in Microvascular Endothelial Cells.
Roy S, Khanna S, Shah H, Rink C, Phillips C, Preuss H, Subbaraju GV, Trimurtulu G, Krishnaraju AV, Bagchi M, Bagchi D, Sen CK.

Laboratory of Molecular Medicine, Department of Surgery, The Ohio State University Medical Centre, Columbus, Ohio.

Inflammatory disorders represent a substantial health problem. Medicinal plants belonging to the Burseraceae family, including Boswellia, are especially known for their anti-inflammatory properties. The gum resin of Boswellia serrata contains bosewellic acids, which inhibit leukotriene biosynthesis. A series of chronic inflammatory diseases are perpetuated by leukotrienes. Although Boswellia extract has proven to be anti-inflammatory in clinical trials, the underlying mechanisms remain to be characterized TNF alpha represents one of the most widely recognized mediators of inflammation. One mechanism by which TNFalpha causes inflammation is by potently inducing the expression of adhesion molecules such as VCAM-1. We sought to test the genetic basis of the antiinflammatory effects of BE (standardized Boswellia extract, 5-Loxin (R) in a system of TNFalpha-induced gene expression in human microvascular endothelial cells. We conducted the first whole genome screen for TNFalpha inducible genes in human microvascular cells (HMEC). Acutely, TNF alpha induced 522 genes and downregulated 141 genes in nine out of nine pairwise comparisons of the 522 genes induced by TNFalpha in HMEC, 113 genes were clearly sensitive to BE treatment. Such genes directly related to inflammation, cell adhesion, and proteolysis. The robust BE sensitive signaling pathways. The use of resources such as Gen MAPP, KEGG and gene ontology led to the recognition of the primary BE sensitive TNFalpha-inducible pathways. BE prevented the TNFalpha-induced expression of matrix metalloproteinases. BE also prevented the inducible expresssion of mediators of apoptosis. Most strikingly, however, TNFalpha-inducible expression of VCAM-1 and ICAM-1 were observed to be sensitive to BE. Realtime PCR studies showed that while TNF alpha potently induced VCAM-1 gene expression, BE completely prevented it. This result confirmed out microarray findings and built and compelling case for the anti-inflammatory property of BE. In an in vivo model of carrageenan-induced rat paw inflammation property of significant antiinflammatory property of BE consistent with our in vitro findings. These findings warant further reserach aimed at indentifying the signalling mechanisms by which BE exerts its anti-inflammatory effects.